Filed under: Ventricular arrhythmias
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Patient: n/a
ECG description:
- Sinus tachycardia
- Supraventricular bigemeny
- One premature ventricular contraction
Discussion:
There is a baseline sinus tachycardia with a PR interval of 130ms, regularly interrupted by premature atrial contractions (PAC). Each PAC depolarizes the atria and resets the SA node, causing a change in automaticity and a noncompensatory extrasystolic pause. Judging by the PR interval as well as P axis and morphology of the premature beats, the ectopic pacemaker is atrial. The ectopic PR interval is 130ms, and it is plausible to think that the ectopic pacemaker is located near the SA node. The P wave axis is ca. 30 degrees, and the ectopic P wave axis is ca. 60 degrees, which means that the atria are depolarized anterogradely and in almost the same direction as from the SA node. QRS axis and morphology is slightly different in the QRS complex following the first premature beat and the second and third. Looking closely, we can see that P wave axis and morphology slightly differs from the first PAC to the next two. The PR interval however is the same. This could be due to multifocality, but since the PR interval is quite similar, the two foci must be very close to each other. After the third bigeminal beat, a broad QRS occurs. In spite of the aberrantly looking RBBB-like morphology, this is most likely a premature ventricular contraction (PVC). If this was aberrancy, it would be due a refractory right bundle branch that couldn’t cope with the rapid changes in automaticity caused by the PAC’s. However, the coupling interval before the broad complex is similar to the other coupling intervals, and this demonstrates that the RBB in fact handles the rapid changes in automaticity quite well. In the precordial leads, we can see a P wave following the PVC, suggesting that the atrias have been depolarized retrogradely from the PVC.
July 1, 2009
Arrhythmias frequently occur in patients undergoing hemodialysis. Shinichi, et al. (American Heart Journal, Vol. 131, Issue 6, 1996:1137-1144) reports that out of 221 patients receiving hemodialysis, a total of 65% (143 pts) had ECG abnormalities, excluding sinus tachycardia and sinus bradycardia. The study looks at ECG abnormalities, not only arrhythmias, and left ventricular hypertrophy has the highest prevalence in the sample group. This was followed by ventricular and supraventricular premature contractions, myocardial ischemia and nonspecific ST-T changes. Additionally, a wide range of other arrhythmias and electrocardiographic abnormalities were seen in the patients. The study discusses probable causes for the rather high prevalence of cardiac disorders and arrhythmias among these patients, but is not fully conclusive in it’s outcome. It points at although arrhythmias commonly appear during hemodialysis, the rather large (65%) prevalence is partly due to baseline cardiac conditions. The results indicate that a combination of changes in intra- and extracellular K levels, changes in other electrolyte levels such as Mg and Ca, rapid correction of metabolic acidosis and decreases of circulating blood volume, appear to trigger arrhythmias in patients with latent cardiac problems.
This case is from a 70 y/o man, initially operated for a perforated ulcus ventriculi. In the postoperative phase, severe sepsis and DIC (Disseminated Intravascular Coagulation) occured, and this participated in a following multiple organ failure including tubuar necrosis and total anuria. His medical history revealed no known cardiac disorders. These ECGs were obtained during a 6 hour session of hemodialysis which involved total fluid removal of 1000 ml.
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The baseline rhythm here is atrial fibrillation with rapid ventricular response. The QRS axis is at 30 degrees. The first beat is a premature ventricular contraction (PVC), which is then followed by two supraventricular beats being aberrantly conducted. The right bundle is still refractory after the PVC, and the following two supraventricular impulses are blocked in the RBB, and are being conducted aberrantly, thus causing a QRS with RBBB morphology.
June 21, 2009
The patient is an 80 y/o woman with known sick sinus syndrome, aortic sclerosis, aortic valve insufficiency, mitral valve insufficiency, tricuspidal valve insufficiency and left ventricular hypertrophy.
About the sick sinus syndrome and the tachy-brady syndrome
There are two types of Sick Sinus Syndrome (SSS): one with and one without associated tachyarrhythmias. SSS is due to many mechanisms related to SA-nodal failure, and in many patients with the syndrome more than one of the mechanisms are present. The most common mechanisms for SSS are severe, persistent sinus bradycardia, sinus arrest, both brief and sustained, with or without initiation of escape pacemakers, sometimes resulting in sustained asystole. Both Stokes-Adams attacks and sudden death is seen with SSS. When SSS is associated with tachyarrhytmhias, this is called the tachy-brady syndrome. Tachy-brady syndrome occurs in more than half of the patients with SSS.¹ The tachy-brady syndrome itself is not a specific condition, but more of a mixture of combinations of arrhythmias. I find it confusing that even the most profilic authors on this subject, as both Marriott² and Chou¹, tend to disagree on whether SSS should be considered part of the tachy-brady syndrome or vice versa. However, there seems to be consistency upon the fact that SSS can occur in two forms, with our without the associated tachycardias. Furthermore the tachy-brady syndrome is usually described as the condition where a tachycardia mechanism is directly associated with the mechanism of a bradycardia or the other way around. One author³ also differentiates between a tachy-brady syndrome and a brady-tachy syndrome, depending on what mechanism that initiates the next.
This series of telemetry strips from the patient described above, show the tachy-brady syndrome in action, manifested by a large and complex cascade of arrhythmic events. Note that there is a baseline first degree AV block at approximately 260 ms.
Note that each strip is not an exact continuation of the strip before it, meaning that i.e. strip number 2 can repeat some of the events in strip 1.
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Top strip: After 4 cycles of sinus bradycardia (43 bpm), atrial flutter occurs. The atrial rate is approximately 260 bpm, and 2:1 AV conduction occurs, resulting in a ventricular rate of 130 bpm. There are F waves (flutter waves) superimposed on each T wave.
Middle strip: Note that this strip is not an exact continuation of strip 1. The first 12 beats are the same. It shows however the atrial flutter persisting with the same AV ratio for several seconds.
Bottom strip: After a while, 4:1 conduction occurs for one cycle. The next cycle is interrupted by a PVC triplet, or a short run of ventricular tachycardia (VT). After the ventricular triplet, the AV node alternates with 2:1 and 3:1 conduction.
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Top strip: Atrial flutter still persists, while 2:1, 3:1 and 4:1 AV conduction occurs successively, before a four beat salvo of premature ventricular contractions occur. Such a salvo would also be considered non-sustained ventricular tachycardia. Following the salvo, AV ratio continues to vary and also with higher degrees of block. 2:1, 3:1 4:1 and 5:1 AV block occurs successively towards the end of the strip.
Middle strip: This strip is almost a repetition of the top strip, and can be ignored.
Bottom strip: Here we can see that even higher degree of AV block occurs, with AV ratio as high as 6:1 before progressively decreasing again.
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Top strip: This strip is recorded at 50mm/s, and shows the baseline atrial flutter being conducted with high degrees of AV block, and interrupted by a 5-beat run of ventricular tachycardia at 140 bpm.
Middle strip: Various degrees of AV block are seen throughout the strip. The deep, negative deflection towards the end is due to a loose electrode.
Bottom strip: AV block continues to vary, here mostly between a 2:1 and 3:1 ratio.
¹ Surawicz, Borys, Chou’s electrocardiography in clinical practice. Philadelphia: Saunders Elsevier, 2006:336-343, 6th edition.
² Wagner, Galen S., Marriott’s Practical Electrocardiography. Philadelphia: Lippincott Williams & Wilkins, 396-404, 10th edition
³ Sandøe, Erik and Bjarne Sigurd, Klinisk Elektrokardiografi. Bingen: Publishing Partners Verlag GmbH, 326-331, 1st edition.
June 18, 2009
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Patient: n/a
ECG description:
- Atrial fibrillation with varied ventricular response – ventricular rate 75-90 bpm
- Axis in the normal quadrant, at ca. 60°
- Early R-wave transition zone (V2)
- T wave inversion in leads inferior leads II, III, aVF and in precordial leads V4-V6
- Multiple and multiform/multifocal premature ventricular contractions (PVC)
- Multiform/multifocal PVC triplet
ECG description:
The three first beats of the ECG are PVCs in rapid succession. They are multiform and each have a different axis. Multiformity should not be considered as 100% specific to multifocality, as beats arising from the same ectopic focus can differ in morphology. However, it is common to both label and consider multiform extrasystoles as multifocal, as multifocality is a much more ominous sign of myocardial irritability. Three consecutive PVCs are per definition a short run of non-sustained ventricular tachycardia. However, the common term is a triplet or a salvo.
May 23, 2009
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Patient: Man, 55 y/o who for several weeks has suffered from strong palpitations, irregular pulse, several near syncopes and fatigue. He explains that the palpitations and the irregular pulse occurs mostly when he is resting. He has noticed that when in physical activity such as i.e. walking up a staircase, the irregular pulse goes away. No medical history otherwise.
ECG description:
- Sinus rhythm
- Intermittent Unifocal Ventricular Bigeminy, the last PVCs have retrograde atrial activation and pseudocompensatory pauses. Read further down in the text for explanation.
- One Ventricular Couplet
- Left Axis Deviation (LAD). Cardiac axis ca -40°
- Left Ventricular Hypertrophy (due to LAD and Sokolow-Lyon voltage criteria)
- T-inversion in lead III, probably non-significant
ECG interpretation: Intermittent Ventricular Bigeminy with Multifocal Ventricular Couplet, LAD and LVH.
ECG comments:
OCCURENCE AND CLINICAL CORRELATION: A bigeminal pattern as this one, falls into the category of complex premature ventricular complexes. This term is used for PVCs that are frequent, multiform, or show bigeminy, trigeminy, couplets, triplets (salvos) or the R on T phenomenon. When PVCs occur as frequent as >30/hour, they are referred to as frequent, according to Lown and Graboys (Chou 2008). Such complexity is part of the clinical correlation, and increases with advancing age. In the early phases of Congestive Heart Failure (CHF), there is often seen even greater increase in frequency of occurence. PVCs can represent an early sign of myocardial hypoxia, but is usually considered benign, unless they compromise cardiac output or trigger more severe tachyarrhythmias as i.e. different types of VT.
MORPHOLOGY AND SITE OF ECTOPY: Looking at the morphology of the PVCs, they clearly arise from the same ectopic focus, hence they are unifocal. The coupling interval is also fixed during the bigeminy. With multifocal/multiform premature complexes, the coupling interval varies due to different locations of the ectopic foci. Here, the ectopic focus is probably located in the right ventricle, as the configuration resembles LBBB pattern. You will note that the extrasystoles are labeled as unifocal and multifocal. Chou, Garcia et al, point to the fact that impulses arising from the same ectopic site can produce complexes of different morphology. Thus, the terms uniformity and multiformity are more correct than unifocality and multifocality. In this case however, the more common term unifocal/multifocal is used.
VENTRICULAR COUPLETS: PVCs may occur in rapid succession, and are named couplets or triplets if two or three (respectively) PVCs follow each other. A triplet is usually referred to as a salvo. Salvos are considered a short run of VT. Unifocal couplets and triplets can be considered normal variants, but clinical correlation should come first here. Multifocal triplets and couplets are a bit more alarming, and can be an early sign of more life-threatening arrhythmias to come. Here, the multifocal/multiform couplet is seen in the second ECG from the top.
INTERMITTENCY AND THE RULE OF BIGEMINY: As defined by Richard Langendorf in 1955, the Rule of Bigeminy describes a pattern where ventricular bigeminy tends to perpetuate itself. The rule is defined by the consequence of PVCs occuring only after appropriately long diastolic intervals. The compensatory pause after a PVC can create conditions for another PVC to occur, and then bigeminy will be perpetuated as long as the compensatory pauses remain sufficiently long. Chou ( 2008 ) describes the rule and says that according to the rule, bigeminy disappears when the heart rate increases. Now, remember that this patient described that the arrhythmia seemed to terminate when under physical activity. If his heart rate increases during activity, this will lead to shorter cycles, which according to Langendorf’s rule may terminate the bigeminy. Then, when at rest again, the heart rate slowes down, apparently creating conditions for the onset of new bigeminy.
THE RULE OF BIGEMINY DISPLAYED:
As seen here, the bigeminy is sustained for five cycles when suddenly interrupted by a ventricular couplet. After the couplet, the underlying sinus rate is increased. This short RR interval seems to terminate the bigeminal pattern, as the second QRS after the couplet is not followed by a PVC. The sinus rhythm then gradually slowes down, probably due to vagal response and/or changes in respiratory rate, and then the diastolic period is appropriately long, the bigeminy reoccurs.
An interesting observation here though, is that the rule seems to be broken in the last ECG, as a new onset of bigeminy occurs after an increase in heart rate. I have not found an explanation for this yet. Comments are welcome.
RETROGRADE ATRIAL ACTIVATION FROM VENTRICULAR ECTOPY AND THE OCCURENCE OF PSEUDOCOMPENSATORY PAUSES
Sometimes, the AV Node allows the ectopic impulse to spread retrogradely back to the atria, although it is often blocked. If the impulse spreads to the atria, a P wave will be created. Since the ectopic depolarization wave is moving from inferior towards superior, the P wave will be inverted on the ECG. In PVCs, such a retrograde P wave is often buried in the QRS, but can also occur immediately after the QRS or have a prolonged RP interval. The RP interval is often long, as cell-to-cell transmission of the ectopic impulse takes time to reach the AV Node. Retrograde P waves occuring with PVCs will have an RP interval longer than or equal to 200ms.
A P wave following a PVC can sometimes be upright (not inverted), and if this is the case, the P wave does not represent retrograde atrial stimulation. Instead, this is the timely P wave marching on through the PVC, not aware of the premature ventricular depolarization. This is AV dissociation, and often occurs with PVCs. If the ectopic impulse is blocked in the AV Node from spreading retrogradely to the atria, the SA Node will not be reset and will keep on pacing as regular. The ventricles though, are still refractory from the premature depolarization, and therefore this sinus P wave will be non-conducted.
Here, the four last PVCs (ECG 3 and 4) are followed by a P wave. The P wave is inverted in positive in aVR and negative in almost all other leads. In some of the complexes, the P wave is biphasic or even positive in lead I and aVL, but the main vector of the P wave is going towards the atrias. This suggests retrograde activation of the atria, and as such the SA Node is also affected and reset. This leads to a change in the sinus cycle, and the postextrasystolic pause becomes longer than expected. Note that with all the PVCs followed by a retrograde P wave, the postextrasystolic pause is longer than expected (Coupling Interval + Postextrasystolic Pause = > Normal Interval x 2). This is called a pseudocompensatory pause, and occurs because retrograde penetration of the AV Node by the premature ventricular impulse prolongs the AV nodal refractoriness and delays the normal anterograde transmission of the next atrial impulse.
January 7, 2009
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ECG description:
- Sinus rhythm
- Multiple premature ventricular complexes (PVC) with varying morphology, appearing in bigeminy pattern (one PVC per normal sinus beat)
- Left Bundle Branch Block due to QRS width 130ms, slurred rS complex in V1, broad R wave in V6.
- Left Axis Deviation. The axis is at approximately -45°
- Normal PR interval: 180 ms
ECG comments:
This is a sinus paced rhythm. The P waves are easiest to spot in V1 and V2. What catches my eye at first, are those big wide beats following each normal sinus beat. These are of course Premature Ventricular Contractions, and are easily recognized (see PVCs explained below). Premature Ventricular Complexes are due to irritable, hypoxic foci in the ventricular tissue, and examining the morphology of these PVCs, they clearly arise from different foci, as they vary in shape and form. They are multiform and therefore multifocal. Look closely, and you can see that all although all the PVCs in this ECG have the same classic PVC configuration, they all look quite different.
PREMATURE VENTRICULAR CONTRACTIONS (PVCs) AND HOW TO SPOT THEM
- Premature (comes earlier than expected compared to the basic sinus cycle)
- Complexes with broad, large and bizarre configuration. Wider, taller and deeper than the normal QRS.
- Not preceded by a P wave. If there is a P wave before an early complex, the possibility is quite large that the focus is atrial.
- Often followed by T wave inversion (due to repolarization disorder)
- Usually a compensatory pause that is twice the regular PP interval
BUT THE 4TH BEAT IS PRECEDED BY A P WAVE! HOW CAN THAT BE A PVC?!
Usually, PVCs are recognized by the fact that they are not preceded by a P wave, which suggests that the electrical focus is ventricular. But there is one exeception to this rule, which is the case of an end-diastolic PVC that occur after the P wave. Remember, the diastole ends when the ventricles contract. The P wave shows atrial contraction and the QRS shows ventricular contraction. Sometimes a PVC can occur at the very end of the diastole, right before they were supposed to contract compared to the previous cycles. Such a PVC will therefore have a P wave preceding it. On the ECG, the P often falls very close to the premature QRS complex, and the PR interval is too short to have conducted this beat. Actually, this P wave is not too early, it is just the normal, regularly scheduled sinus beat coming on time. It just happens to fall right before a premature ventricular contraction.
The fourth beat in this ECG is a PVC preceded by a P wave, but is still a PVC. The preceding P wave is just the timely P wave from the sinus node that fires regularly.
POST-EXTRASYSTOLIC PAUSES: COMPENSATORY AND NON-COMPENSATORY
The cycle pause after a PVC is called a post-extrasystolic pauses. Such pauses are divided into two kinds: Compensatory Post-Extrasystolic Pauses and Non-Compensatory Post-Extrasystolic Pauses. These names are often too long to use, so the terms compensatory pause and non-compensatory pause are used instead.
Compensatory Post-Extrasystolic Pause
A PVC starts in the ventricles from an irritable, often hypoxic focus. Therefore, it only depolarizes the ventricles, not the SA Node. Therefore, the SA Node is not reset. So the SA Node fires as planned and on schedule. Often, if you use your caliper and measure PP intervals, you can spot that timely P within a PVC. The problem is though, that when the sinus node fires, the ventricles are still refractory, and the sinus impulse doesn´t get conducted. When this impulse reaches the ventricles, they´re not ready, and can´t depolarize. So there is a pause after the PVC as the ventricles finish repolarizing, making them receptive to the next sinus generated cycle. Remember that since the depolarization begins in the ventricular tissue, the SA Node will never know anything about this premature impulse. And if it doesn´t get depolarized by the impulse, it will not reset and will keep on pacing. And if the SA Node is not reset, the compensatory pause will be an exact multiple of the regular PP interval. So by measuring PP intervals, you can check if the pause is compensatory or not.
Non-Compensatory Post-Extrasystolic Pause
With non-compensatory pauses, the SA Node is reset and starts a new sinus cycle. The non-compensatory pause is not an exact multiple of the regular PP interval. The SA Node is usually reset by Premature Atrial Contractions (PACs) or Premature Junctional Contractions (PJCs). PVCs are sometimes followed by a non-compensatory pause, but only very rarely. Remember, for the SA Node to be depolarized by a PVC, there will have to be retrograde conduction through the AV Node. This is not very usual, but can happen. The take-home advice here, is that with non-compensatory pauses, you are usually dealing with a PAC or a PJC.
November 28, 2008
Patient: n/a
ECG description:
- Sinus rhythm at 85 bpm
- Ventricular extra systoles in trigeminy pattern. Every third beat is a Premature Ventricular Complex (PVC).
- Marked First Degree AV Block. PR interval is 310 ms.
- Incomplete Left Bundle Branch Block (LBBB). QRS width 100ms.
- Axis normal at approx. 60°
ECG diagnosis: Ventricular trigeminy with marked (severe) 1° AV Block and incomplete LBBB.
ECG Comments:
PVC TRIGEMINY: When every third beat is a PVC, the term trigeminy is used. The PVCs here are unimorph and therefore unifocal, which means they all have the same morhpology and therefore arise from the same ectopic focus. Premature beats originates in irritable autmaticity foci that fires spontaneously. Such beats come earlier than expected in the rhythm. It is also important to understand that although PVCs in many ways are considered to be benign, they are early signs of hypoxia. 6 PVCs per minute is considered pathological. Remember that a continuous run of bigeminy or trigeminy will quickly exceed that criteria, and will then usually indicate that a very irritable focus is hypoxic and needs attention.
1° AV BLOCK: The PR interval in this ECG is 310ms. This is a so called marked First Degree AV Block. This term indicates that the PR interval is markedly prolonged. This is noted because sometimes the AV conduction delay becomes so severe that pacemaker insertion may be needed. I am not completely sure about the exact criteria here, but from what I have read permanent pacing is indicated when the patient is symptomatic and when the PR interval exceeds 300ms. This article from Emergency Medicine News discusses the matter, and says that those with a PR interval >300ms are at risk of developing complete heart block.
INCOMPLETE LBBB: The morphology here resembles LBBB, but the QRS is only 100ms. To diagnose BBB, the QRS complex must be at least 120 ms. Therefore, this LBBB must be considered incomplete.
November 19, 2008
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Short anamnesis: Male patient, around 70 years of age. Admitted to the ER with ARF (acute renal failure). Serum potassium (kalium) levels at the time of the ecg recording were 7.8 mmol/l.
ECG description:
- Sinus rhythm, approx. 75 bpm
- Normal axis (although deviated towards the left at approx. 0°)
- Tall, tented/peaked T waves.
- One PVC (premature ventricular complex) at the end of the recording
Comments: With severe hyperkalemia like this, one would perhaps also suspect to find a widening of the QRS complex and small P waves, which would be a classic presentation. The QRS in this ecg seems to be normal at about 80ms. The P-waves also seem normal.
November 7, 2008
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Short anamnesis: Male patient, ca. 60 years old. Sudden onset of palpitations, general discomfort, light-headedness and near-syncopes. Normotensive.
ECG description:
- Sinus rhythm with varied rate
- Normal cardiac axis around 0°
- Premature ventricular complexes (PVC) in bigeminal pattern
November 3, 2008
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Anamnesis:
30 year old man with acute chest pain onset within three hours. The pain is dull and constant in the middle of his chest, and radiates towards and over his left shoulder. The intensity of the pain seems to relate to his body position, as it gets worse by lying down and improves by sitting up. He has has a mild fever and presents with fatigue and general weakness.
ECG description:
- Sinus rhythm, 110bpm
- Ventricular bigeminy: Repeated pattern of one PVC for each sinus beat.
- Global ST-elevation: ST-segments slightly elevated in V1-V6, I, II, III, aVF
- Left ventricular hypertrophy due to Sokolow-Lyon index: S in V1 + R in V5 > 35mm
- Normal axis, approx. 60°
Conclusion:
Global ST-elevation together with the patient´s clinical presentation correlates with pericarditis. The PVC pattern could suggest that the myocardium has been affected secondary to the pericarditis, and therefore this ECG could show signs of a myopericarditis.
October 18, 2008